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3 results on '"a sequence"'

1. Characteristics of the a sequence of the duck Plague virus genome and specific cleavage of the viral genome based on the a sequence

Author

Qiao Yang, Yaya Feng, Yuanxin Zhang, Mingshu Wang, Renyong Jia, Dekang Zhu, Shun Chen, Mafeng Liu, Xinxin Zhao, Ying Wu, Shaqiu Zhang, Bin Tian, Xumin Ou, Sai Mao, Juan Huang, Qun Gao, Di Sun, Zhen Wu, Yu He, Ling Zhang, Yanling Yu, and Anchun Cheng

Subjects
Duck plague virus, a sequence, cleavage and packaging of viral genome, TaqMan dual qRT‒PCR, Veterinary medicine, SF600-1100
Abstract

Abstract During the replication process, the herpesvirus genome forms the head-to-tail linked concatemeric genome, which is then cleaved and packaged into the capsid. The cleavage and packing process is carried out by the terminase complex, which specifically recognizes and cleaves the concatemeric genome. This process is governed by a cis-acting sequence in the genome, named the a sequence. The a sequence and genome cleavage have been described in some herpesviruses, but it remains unclear in duck plague virus. In this study, we analysed the location, composition, and conservation of a sequence in the duck plague virus genome. The structure of the DPV genome has an a sequence of (DR4)m-(DR2)n-pac1-S termini (32 bp)-L termini (32 bp)-pac2, and the length is 841 bp. Direct repeat (DR) sequences are conserved in different DPV strains, but the number of DR copies is inconsistent. Additionally, the typical DR1 sequence was not found in the DPV a sequence. The Pac1 and pac2 motifs are relatively conserved between DPV and other herpesviruses. Cleavage of the DPV concatemeric genome was detected, and the results showed that the DPV genome can form a concatemer and is cleaved into a monomer at a specific site. We also established a sensitive method, TaqMan dual qRT‒PCR, to analyse genome cleavage. The ratio of concatemer to total viral genome was decreased during the replication process. These results will be critical for understanding the process of DPV genome cleavage, and the application of TaqMan dual qRT‒PCR will greatly facilitate more in-depth research.

Published
2024
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2. Characteristics of the a sequence of the duck Plague virus genome and specific cleavage of the viral genome based on the a sequence.

Author

Yang, Qiao, Feng, Yaya, Zhang, Yuanxin, Wang, Mingshu, Jia, Renyong, Zhu, Dekang, Chen, Shun, Liu, Mafeng, Zhao, Xinxin, Wu, Ying, Zhang, Shaqiu, Tian, Bin, Ou, Xumin, Mao, Sai, Huang, Juan, Gao, Qun, Sun, Di, Wu, Zhen, He, Yu, and Zhang, Ling

Abstract

During the replication process, the herpesvirus genome forms the head-to-tail linked concatemeric genome, which is then cleaved and packaged into the capsid. The cleavage and packing process is carried out by the terminase complex, which specifically recognizes and cleaves the concatemeric genome. This process is governed by a cis-acting sequence in the genome, named the a sequence. The a sequence and genome cleavage have been described in some herpesviruses, but it remains unclear in duck plague virus. In this study, we analysed the location, composition, and conservation of a sequence in the duck plague virus genome. The structure of the DPV genome has an a sequence of (DR4)m-(DR2)n-pac1-S termini (32 bp)-L termini (32 bp)-pac2, and the length is 841 bp. Direct repeat (DR) sequences are conserved in different DPV strains, but the number of DR copies is inconsistent. Additionally, the typical DR1 sequence was not found in the DPV a sequence. The Pac1 and pac2 motifs are relatively conserved between DPV and other herpesviruses. Cleavage of the DPV concatemeric genome was detected, and the results showed that the DPV genome can form a concatemer and is cleaved into a monomer at a specific site. We also established a sensitive method, TaqMan dual qRT‒PCR, to analyse genome cleavage. The ratio of concatemer to total viral genome was decreased during the replication process. These results will be critical for understanding the process of DPV genome cleavage, and the application of TaqMan dual qRT‒PCR will greatly facilitate more in-depth research. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
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3. Replication and recombination in cells infected with Herpes simplex virus type 1

Author

Yao, Xiao-Dan 1958

Subjects
topoisomerase II, a sequence, viruses, RAD51, homologous recombination, DNA replication, HSV-1, linear DNA
Abstract

The studies presented in this thesis have been performed in order to improve our understanding of the molecular background of HSV-1 DNA metabolism. Specifically, it attempts to address the role of homologous recombination in the viral life cycle and to identify host enzymes that take part in viral DNA metabolism. We investigated the effects of ICRF-193, an inhibitor of topoisomerase II, on the replication of HSV-1. Then we examined mechanisms of recombination in cells infected with HSV-1 to establish the mechanism of circularization of HSV-1 genome. Finally, we investigated the coupling between HSV-1 DNA replication and homologous recombination as well as requirements for cellular gene products in homologous recombination. Plasmids containing HSV-1 oriS were constructed as the substrates for viral replication and recombination. Uninfected and HSV-1 infected cells with different genetic backgrounds were used. Transient replication assays were utilized to detect virus-dependent DNA replication and recombination. Furthermore, two other assays were developed for detecting homologous recombination: recombination-dependent expression of luciferase and recombination between HSV-1 tsS and tsK strains. To study the enzymatic background of homologous recombination HSV-1 amplicons were used to express recombination genes in human cells.We found that HSV-1 replication was specifically inhibited by ICRF-193 early in infection suggesting that topoisomerase II decatenates early replication intermediates. We have seen that linear DNA provided with directly repeated HSV-1 a sequences at the ends replicated as efficiently as circular DNA. The results indicate that linear HSV-1 DNA might be circularized by a sequences-mediated homologous recombination before replication. The reaction was not dependent on XPF/ERCC4 protein, suggesting that it does not proceed by a single strand-annealing pathway. Homologous recombination occurred also in absence of HSV-1 dependent DNA replication and viral gene products, which implies that DNA replication and homologous recombination may be coordinated but mechanistically independent events. We also demonstrated that homologous recombination was cell type dependent. Linear DNA with non-homologous ends induced p53 dependent apoptosis and failed to recombine in Balb/c 3T3 cells. It appears that homologous recombination is controlled by p53. Furthermore, homologous recombination may protect HSV-1-infected cells from initiating apoptosis and stimulate viral DNA replication.Finally, homologous recombination of replicating HSV-1 genomes was profoundly reduced by overexpression of a non-functional RAD51 in human primary fibroblasts. Our results suggest that RAD51 dependent homologous recombination is an important, but not necessarily exclusive, mechanism for promoting recombination of replicating HSV-1 DNA.

Published
1999

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